Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Study of PRMT5 mediated H3R2me2s in Th1-like iTregs

ABSTRACT: In this study, we have studied the genes associated with PRMT5 mediated histone methylation (H2R2me2s) in Th1-like iTregs. This particular epigenetic markers is upregulated in Th1 cells, and Th1-like iTregs. Therefore, we wanted to identify the genes H3R2me2s is regulating in Th1-like iTregs as compared to iTregs or Th1 cells. The goal of this sequencing was to identify if H2R2me2s is important for increased suppressive capacity of Th1-like iTregs or not.

ORGANISM(S): Mus musculus

PROVIDER: GSE243686 | GEO | 2023/12/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression analysis of iTregs and nTregs

Project description:MBP TCR Tg mouse (1B3) generates only iTregs when crossed onto RAGKO background. Tregs from 1B3.RAG mouse were used for gene expression analsysis to determine genes selectively expressed in peripherally generated iTregs iTregs from 1B3.RAG mice (>90% Foxp3+) were run against total Tregs from 1B3 and WT NOD mice. Foxp3- CD4+T cells were used as control from all strains as Tconv. (1B3 denotes MBP-TCR Tg mouse).

2013-07-03 | E-GEOD-39724 | biostudies-arrayexpress

Gene expression analysis of iTregs and nTregs

2013-07-03 | GSE39724 | GEO

Sustained store-operated calcium entry utilizing activated chromatin state leads to instability in iTregs

Project description:Thymus-originated tTregs and in vitro induced iTregs are subsets of regulatory T cells. While they share the capacity of immune suppression, their stabilities are different, with iTregs losing their phenotype upon stimulation or under inflammatory milieu. Epigenetic differences, particularly methylation state of Foxp3 CNS2 region, provide an explanation for this shift. Whether additional regulations, including cellular signaling, could directly lead phenotypical instability requires further analysis. Here we show that upon TCR triggering, store-operated calcium entry (SOCE) and NFAT nuclear translocation are blunted in tTregs, yet fully operational in iTregs, similar to Tconvs. On the other hand, tTregs show minimal changes in their chromatin accessibility upon activation, in contrast to iTregs that demonstrate an activated chromatin state with highly accessible T cell activation and inflammation related genes. Assisted by several cofactors, NFAT driven by strong SOCE signaling in iTregs preferentially binds to primed opened T helper (TH) genes, resulting in their activation normally observed only in Tconv activation, ultimately leads to instability. Conversely, suppression of SOCE in iTregs can partially rescue their phenotype. Thus our study adds two new layer, cellular signaling and chromatin accessibility, of understanding in Treg stability, and may provide a path for better clinical applications of Treg cell therapy.

2023-11-01 | GSE246431 | GEO

PRMT5-regulates developmental myelination

Project description:PRMT5 is important for gliomas, however its physiological function in oligodendrocyte progenitors (OPCs), remains poorly understood. Here we report PRMT5 to be responsible for symmetric di-methylation of histone H4R3 (H4R3me2s) in OPC. PRMT5 depletion via CRISPR/Cas9 decreased H4R3me2s, altered the OPC transcriptome, and decreased OPC survival. Strikingly, these changes were associated with a marked increase of H4K5ac in OPC, but not in gliomas. Consistently, ChIP-sequencing analysis revealed increased genome-wide distribution of H4K5ac in PRMT5 knockout cells. In vitro acetylation assays demonstrated reciprocal inhibition between symmetric arginine methylation and lysine acetylation. Low H4R3me2s and high H4K5ac levels were also detected in OPC in mice with lineage-specific ablation of Prmt5 (Olig1-Cre;Prmt5fl/fl), resulting in severely impaired developmental myelination. Importantly, pharmacological inhibition of acetyltransferase activity partially rescued the effect of Prmt5 deletion on oligodendrocyte-specific gene transcripts. Collectively, we identify PRMT5 as a critical modulator of histone acetylation and OPC differentiation in early developmental myelination.

2018-06-02 | GSE94067 | GEO

PRMT5 is essential for sustaining normal adlut hematopoiesis

Project description:Examining the effects of PRMT5 loss on the gene expression profile of hematopoietic stem and progenitor cells We established the PRMT5 conditional KO mice, and bred the mice with Mx1 cre transgenic mice to delete PRMT5 in hematopoietic cells. We isolated hematopoetic stem and progenitor cells 3 days after PRMT5 deletion, and examined the gene expression files using RNA-sequencing.

2015-07-15 | E-GEOD-69937 | biostudies-arrayexpress

PRMT5 knockdown changes gene expression in prostate cancer cells

Project description:PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine. Recent reports have indicated that PRMT5 is overexpressed in multiple cancer types, including prostate. However, the exact contribution of PRMT5 to prostate tumorigenesis is unknown. To explore the functional role of PRMT5 in prostate cancer (PCa), we knocked down PRMT5 by lentiviral shRNAs in both AR-dependent LNCaP cells and AR-independent PC3 cells. Our data suggests that PRMT5 regulates PCa cell biology. To further identify PRMT5-regulated genes in PCa, we performed paired-end RNA-seq analysis in PC3 and LNCaP cells with or without PRMT5-knockdown.

2023-12-25 | GSE117596 | GEO

PRMT5 genomic deregulation supports growth and stress tolerance in chronic lymphocytic leukemia

Project description:Patients suffering from chronic lymphocytic leukemia (CLL) display highly diverse clinical courses ranging from indolent cases to aggressive disease with genetic and epigenetic features resembling this diversity. Here, we developed a comprehensive approach combining a variety of molecular and clinical data to identify translocation events disrupting long-range chromatin interactions and causing cancer-relevant transcriptional deregulation. Thereby, we identified a B cell specific cis-regulatory element restricting the expression of genes in the associated locus, including PRMT5 and DAD1, two factors with oncogenic potential. Examining the role of PRMT5 in CLL identified transcriptional programs associated with pathways of stress tolerance and growth support, maintaining MYC-driven gene expression in vivo and in vitro. Conversely, inhibition of PRMT5 impairs factors involved in DNA-repair and sensitizes cells for apoptosis. Finally, we show that artificial deletion of the regulatory element from its endogenous context resulted in upregulation of corresponding genes, including PRMT5. Furthermore, such disruption renders PRMT5 transcription vulnerable to additional stimuli and subsequently also alters the expression of downstream PRMT5 targets.

2020-08-19 | E-MTAB-8219 | biostudies-arrayexpress

PRMT5 genomic deregulation supports growth and stress tolerance in chronic lymphocytic leukemia

2020-08-19 | E-MTAB-8203 | biostudies-arrayexpress

RNA-seq analysis of PRMT5 targeted genes in Tu212 cells

Project description:RNA-sequencing was performed to identify the possible underlying signaling pathway of PRMT5 overexpressing in Tu212 cells. Cells were treated with pEZ-PRMT5 or pEZ-Vector.

2020-08-08 | GSE155879 | GEO

RNA sequencing analysis of wild-type and Scd1-deficient CD4+ early iTregs

Project description:Analysis of differentially expressed genes in CD4+ early iTregs isolated from wild-type and Scd1-deficient mice. The goal of this study was to elucidate the effect of Scd1 on Treg differentation.

2023-02-13 | GSE224839 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data